title: Muscle blood flow at onset of dynamic exercise in humans.
abstract: To evaluate the temporal relationship between blood flow, blood pressure, and muscle contractions, we continuously measured femoral arterial inflow with ultrasound Doppler at onset of passive exercise and voluntary, one-legged, dynamic knee-extensor exercise in humans. Blood velocity and inflow increased (P < 0.006) with the first relaxation of passive and voluntary exercise, whereas the arterial-venous pressure difference was unaltered [P = not significant (NS)]. During steady-state exercise, and with arterial pressure as a superimposed influence, blood velocity was affected by the muscle pump, peaking (P < 0.001) at approximately 2.5 +/- 0.3 m/s as the relaxation coincided with peak systolic arterial blood pressure; blood velocity decreased (P < 0.001) to 44.2 +/- 8.6 and 28.5 +/- 5.5% of peak velocity at the second dicrotic and diastolic blood pressure notches, respectively. Mechanical hindrance occurred (P < 0.001) during the contraction phase at blood pressures less than or equal to that at the second dicrotic notch. The increase in blood flow (Q) was characterized by a one-component (approximately 15% of peak power output), two-component (approximately 40-70% of peak power output), or three-component exponential model (> or = 75% of peak power output), where Q(t) = Qpassive + delta Q1.[1 - e-(t - TD1/tau 1)]+ delta Q2.[1 - e-(t - TD2/tau 2)]+ delta Q3.[1 - e-(t - TD3/tau 3)]; Qpassive, the blood flow during passive leg movement, equals 1.17 +/- 0.11 l/min; TD is the onset latency; tau is the time constant; delta Q is the magnitude of blood flow rise; and subscripts 1-3 refer to the first, second, and third components of the exponential model, respectively. The time to reach 50% of the difference between passive and voluntary asymptotic blood flow was approximately 2.2-8.9 s. The blood flow leveled off after approximately 10-150 s, related to the power outputs. It is concluded that the elevation in blood flow with the first duty cycle(s) is due to muscle mechanical factors, but vasodilators initiate a more potent amplification within the second to fourth contraction.
authors.affiliation: Copenhagen Muscle Research Centre, Rigshospitalet, Denmark.
authors.forename: G
authors.initials: G
authors.lastname: Rådegran
authors.forename: B
authors.initials: B
authors.lastname: Saltin
mesh_terms: D000328:Adult; D001783:Blood Flow Velocity; D001794:Blood Pressure; D015444:Exercise / Q000502:physiology; D005263:Femoral Artery / Q000502:physiology*; D006801:Humans; D007719:Knee Joint; D008297:Male; D009119:Muscle Contraction / Q000502:physiology*; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000502:physiology; D005082:Physical Exertion / Q000502:physiology*; D012039:Regional Blood Flow; D013997:Time Factors